Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

ABSTRACT: Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

PROVIDER: PRJNA1041459 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26855603_1.fastq.gz	Fastqsanger.gz
	SRR26855603_2.fastq.gz	Fastqsanger.gz
	SRR26855604_1.fastq.gz	Fastqsanger.gz
	SRR26855604_2.fastq.gz	Fastqsanger.gz
	SRR26855605_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

Project description:Idiopathic nephrotic Syndrome (NS) is a common glomerular disease. While glucocorticoids (GC) are the primary treatment, the PPARγ agonist pioglitazone (Pio) also reduces proteinuria in patients with NS and directly protects podocytes from injury. Since both drugs reduce proteinuria, we hypothesized these effects result from overlapping transcriptional patterns. Systems biology approaches compared glomerular transcriptomes from rats with PAN-induced NS treated with GC vs. Pio and identified 29 commonly regulated genes-of-interest, primarily involved in extracellular matrix (ECM) remodeling. Correlation with clinical idiopathic NS patient datasets confirmed glomerular ECM dysregulation as a potential mechanism of injury. Cellular deconvolution in silico revealed GC- and Pio-induced amelioration of altered genes primarily within podocytes and mesangial cells. While validation studies are indicated, these analyses identified molecular pathways involved in the early stages of NS (prior to scarring) suggesting that targeting glomerular ECM dysregulation may enable a future non-immunosuppressive approach for proteinuria reduction in idiopathic NS.

2024-12-01 | GSE248053 | GEO

Glucocorticoid- and pioglitazone-induced proteinuria reduction in experimental NS both correlate with glomerular ECM modulation.

Project description: Not available

| S-EPMC10770536 | biostudies-literature

Tcf21 deletion from podocyte precursors as a model for congenital nephrotic syndrome

Project description:Here, we establish a mouse model of congenital nephrotic syndrome (NS) by genetic deletion of transcription factor 21 (Tcf21), a gene required for normal podocyte development, selectively from early podocyte precursors. Single cell transcriptomics of kidneys from these mice capture glomerular and tubulointerstitial changes that occur early in the course of NS and provide additional insights into: 1) the regulation of podocyte development and function by TCF21, 2) the effects of podocyte injury on other glomerular cells, and 3) the tubulointerstitial changes that occur in response to the glomerular dysfunction and associated massive proteinuria of podocytopathies.

2026-05-04 | GSE311499 | GEO

Protective role of early Tnfsf15 upregulation in limiting glomerular injury and proteinuria in experimental Alport Syndrome

Project description:Alport syndrome is a progressive kidney disease caused by pathogenic variants in genes encoding type IV collagen, a major structural component of the glomerular basement membrane (GBM). Abnormal GBM architecture impairs filtration and triggers inflammation, fibrosis, and eventual kidney failure. Because disease progression is irreversible, identifying early molecular changes is essential for understanding disease onset. We performed glomerular single-cell RNA sequencing (scRNA-seq) in a Col4a5 G5X Alport mouse model at 5 weeks of age, prior to detectable proteinuria or GBM/podocyte abnormalities (pre-onset), and at 8 weeks, when mild proteinuria and structural defects emerged. Despite the early stage, scRNA-seq revealed widespread transcriptional alterations, most prominently in podocytes. Among genes upregulated at both time points, we identified Tumor Necrosis Factor Superfamily Member 15 (Tnfsf15), previously associated with kidney disease susceptibility but with unclear function. To determine its role in Alport syndrome, we generated Tnfsf15-deficient Alport mice. Tnfsf15 homozygous knockout mice exhibited increased proteinuria and exacerbated glomerular injury compared with Tnfsf15(+/+) Alport mice during early disease. These findings support a protective role for Tnfsf15 in the early stages of Alport syndrome, mitigating proteinuria and limiting glomerular injury.

2026-03-22 | GSE318380 | GEO

Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

Project description:Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

| PRJNA903394 | ENA

Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

Project description:Proteinuria is a cardinal feature of glomerular diseases and an important risk factor for tubulo-interstitial damage, progressive decline in kidney function, and cardiovascular complications, but the precise effects of proteinuria on tubules were previously unclear. Here, using an established mouse model of glomerulopathy, single cell sequencing, in vivo imaging and other complementary methods, we investigate in detail the spatiotemporal landscape of genetic responses to increased protein filtration along the nephron. We show that proteinuria is a potent modulator of cell signaling in tubules, and triggers extensive genetic reprogramming in distal segments, with activation of numerous developmental pathways, and a generalized convergence and loss of differentiation markers. Meanwhile, in the proximal tubule - where filtered proteins are normally endocytosed and degraded - we find that encroachment of protein uptake from early (S1) into later (S2) segments causes substantial remodeling of the latter, with dramatic downregulation of canonical processes such as organic anion/uremic toxin secretion and lipid metabolism, and a concomitant increase in reabsorptive markers. Thus, we demonstrate that the tubular effects of proteinuria are extensive, pleotropic and segment specific. Moreover, we identify protein exposure as an important environmental cue that shapes the axial topography of the nephron. Taken together, these findings could explain some well recognized phenomena in humans with chronic kidney disease (CKD).

2024-05-06 | GSE218376 | GEO

Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model

2009-08-26 | GSE12599 | GEO

Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists [ADR]

Project description:Nephropathy was induced with puromycin amino-nucleoside (PAN) in Wistar rats and treated with daily treatments of Pioglitazone (Pio) and GQ-16. Nephropathy was induced in a separate group of rats with Adriamycin (ADR) in Wistar rats. Total glomerular RNA was isolated, and mRNA libraries were generated and subjected to sequencing using NovaSeq6000 SP. Injury with PAN and ADR resulted in differential expression of genes (DEGs). Many of the PAN-induced DEGs were restored with Pio and GQ16 treatments.

2025-06-02 | GSE286014 | GEO

Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model

Project description:The pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown. To gain insight into the pathogenesis of proteinuria development, we characterized the glomerular gene expression changes that accompany early stages of proteinuria induced by lipopolysaccharide (LPS) in mice. Nine-week-old female C57Bl6 mice were allocated to LPS-treated group (n=6) or PBS control group (n=4), and subsequently treated either by a single intraperitoneal injection LPS or control buffer.

2009-08-25 | E-GEOD-12599 | biostudies-arrayexpress

Glomerular voom-transformed RNAseq counts from the Neptune Cohort and healthy living donors [re-analysis of GSE197307]

Project description:Glomerular Transcriptome in the Nephrotic Syndrome study network cohort

2024-02-07 | GSE254957 | GEO